Good Calories, Bad Calories

in 1980—equivalent to the yearly per-capita consumption recorded in the United States or in the United Kingdom a century earlier.

The remarkable health of the islanders of Crete and Corfu in Keys’s Seven Countries Study—and thus the supposedly salubrious effects of the Mediterranean diet itself—could also be explained by the lack of sugar and white flour. Despite the popularity of the Mediterranean diet today, our understanding of what exactly such a diet is—particularly in Crete and Corfu, where Keys’s study had documented such remarkably low mortality rates—is based on only two dietary surveys: Keys’s study itself, which analyzed the Cretan diet in 1960, and a Rockefeller Foundation study in 1947. According to the Seven Countries Study, the Cretan diet circa 1960 included a total of only sixteen pounds a year of sugar, honey, pastries, and ice cream. According to the Rockefeller study, the Cretan diet included only ten pounds a year of sugar and sweets, and the considerable bread consumed was all wholemeal. The reported benefits of the Mediterranean diet, therefore, could be attributed to the fish, olive oil, and vegetables consumed, as it is today, but they could also be due to the minimal quantities of sugar and the absence of white flour.

This lack of concern for any potential health-related difference between vegetables and starches, on the one hand, and refined starches and sugars, on the other, has haunted cancer research as well. Speculation that dietary fat caused breast, colon, and prostate cancer began in the 1970s, with the same international comparisons that led to the heart-disease hypothesis in the 1950s. Cancer epidemiologists simply compared carbohydrate, protein, and fat contents of diets in different countries with the mortality from various cancers. And these investigators, too, concluded that differences in cancer rates could be explained by differences in fat consumption and animal-fat consumption, particularly between Japan and the United States. They did not serve science well by ignoring sugar consumption and the difference between refined and unrefined carbohydrates.

These preliminary studies then prompted hundreds of millions of dollars of studies that failed to confirm the initial hypothesis that fat or animal fat led to cancer. (Even in the past few years, similar studies have attributed rising cancer rates in China to the increased consumption of fat, while again paying no attention to sugar or the refinement of the carbohydrates in the diets.) In 1975, Richard Doll and Bruce Armstrong published a seminal analysis of diet and cancer, in which they noted that, the higher the sugar intake in different nations, the higher both the incidence of and mortality from cancer of the colon, rectum, breast, ovary, uterus, prostate, kidney, nervous system, and testicles.^*35 Still, epidemiologists fixated on the fat-cancer hypothesis and made no attempt to measure the refined carbohydrates in the populations they studied. As a result, a joint 1997 report of the World Cancer Research Fund and the American Institute for Cancer Research, entitled Food, Nutrition and the Prevention of Cancer, said this:

The degree to which starch is refined in diets, particularly when the intake of starch is high, may itself be an important factor in cancer risk, as may the volume of refined starches and sugars in diets. Epidemiological studies have not, however, generally distinguished between degrees of refining or processing of starches, and there are, as yet, no reliable epidemiological data specifically on the effects of refining on cancer risk.

Cleave’s saccharine-disease hypothesis may be intuitively appealing, but it is effectively impossible to test without a randomized controlled trial. If Cleave was right, then epidemiologists comparing populations or individuals with and without chronic disease have to take into account not just sugar consumption but flour, and whether that flour is white or whole-grain, and whether rice is polished or unpolished, white or brown, and even how much beer is consumed compared with, say, red wine or hard liquor. They might have to distinguish between table sugar and the sugar in soft drinks and fruit juices. Just as fats are now divided into saturated, monounsaturated, and polyunsaturated (and, ideally, into the various subcategories, including stearic acid and oleic acid), carbohydrates have to be separated into subcategories as well. It would be easy, Cleave suggested, to gather together the twenty fattest people in any neighborhood and find that “they wouldn’t have a sweet tooth among them, and they wouldn’t like sugar”—they would all be beer drinkers. “Beer is full of malt sugar and enormously fattening,” he said.

It may have been these complications that led indirectly to a pared-down version of Cleave’s hypothesis—one that would receive far more publicity—blaming coronary heart disease, diabetes, and other chronic diseases effectively on sugar alone. So said John Yudkin, who, unlike Cleave, was a prominent figure in the nutrition-research community. In 1953, he had founded the department of nutrition at Queen Elizabeth College in London, the first dedicated department of nutrition in Europe. In the late 1950s, Yudkin began advocating a very low-carbohydrate diet for weight loss and wrote a popular diet book, This Slimming Business. He believed starches and sugars brought nothing of nutritional importance to the diet except calories—sugar was the worst offender—and so they were the obvious nutrient to remove from a weight-loss diet.

Yudkin entered the heart-disease debate in 1957, after Keys published his first series of papers claiming a “remarkable relationship” between fat consumption and coronary heart disease. Yudkin was among those who had taken Keys to task for the limitations of his analysis and his overinterpretation of very limited and unreliable data. Yudkin noted that many factors correlate with heart-disease deaths (not just dietary-fat consumption) one of which happened to be sugar consumption. Yudkin paid attention only to the trends of diet and disease in developed nations, and to heart disease and obesity, rather than the whole slew of chronic diseases, and he decided that sugar itself was the fundamental problem. (Yudkin would distance himself from Cleave by refusing to use the term “refined carbohydrates,” because it “gives the impression that white flour has the same ill effects as sugar,” which he considered grossly misleading.) Through the 1960s, Yudkin published the results of a series of experiments implicating sugar in heart disease. He fed sugar and starch to rats, mice, chickens, rabbits, and pigs, and reported that the sugar, depending on the particular animal involved, raised some combination of cholesterol, triglycerides, and insulin levels. Triglycerides are a form of fat molecule found in the blood, and a series of researchers beginning with Pete Ahrens at Rockefeller University and Margaret Albrink of Yale had suggested that triglyceride levels were a better predictor of heart disease than was cholesterol. (Diabetics, as Joslin had noted, all too often died of atherosclerosis, and they, too, inevitably had high levels of triglycerides.) Yudkin also fed high-sugar diets to college students and reported that it raised their cholesterol and particularly their triglycerides; their insulin levels rose, and their blood cells became stickier, which he believed could explain the blood clots that seemed to precipitate heart attacks.

By the early 1970s, the medical-research community was taking Yudkin’s hypothesis seriously. But now the very existence of Keys’s hypothesis was the primary obstacle to the acceptance of Yudkin’s. If one was right, than the other was very likely wrong. The European research community tended to be open-minded on this question. “Although there is strong evidence that dietary fats, particularly the saturated ones, play an important role in the etiology of [coronary heart disease], there is no proof that they are the only or the main culprit,” wrote Roberto Masironi, an Italian cardiologist who would become president of the European Medical Association. “As regards the relationship of sugars to cardiovascular diseases, it must be borne in mind that these nutrients have common metabolic pathways with fats. Disturbances in carbohydrate metabolism may be responsible for abnormal fat metabolism and may therefore act as a causative factor in the development of atherosclerosis and of coronary disease.”

In the United States, however, Keys’s hypothesis ruled. Keys himself went after Yudkin in a letter that he first distributed widely to investigators in 1970, before it was published in the journal Atherosclerosis. Keys called Yudkin’s arguments for the role of sugar in heart disease “tendentious” and his evidence “flimsy indeed” he treated Yudkin as a figure of ridicule. What made Keys’s critique so ironic, though, is that virtually every argument that he invoked to criticize Yudkin’s hypothesis had been used in the past as criticism of his own. Most were equally valid for both, and spoke to the flaws in the epidemiologic evidence—the use of international cause-of-death statistics and food-consumption data or dietary-recall surveys to draw conclusions about cause and effect—rather than to the actual validity of the hypotheses. Keys’s case against Yudkin eventually came to rest almost entirely on his invocation of the Seven Countries Study as support for his hypothesis. In fact, the Seven Countries Study had been one of the very few studies that had measured sugar consumption in its populations, and sugar indeed turned out to predict heart-disease rates